THE ROLE OF GLUCAGON ADMINISTRATION IN THE DIAGNOSIS AND TREATMENT OFPATIENTS WITH TUMOR HYPOGLYCEMIA

BACKGROUND. Tumor hypoglycemia can be recurrent and severe enough to i nterfere with definitive antineoplastic treatment. Therefore, rapid co mmencement of effective therapy is essential. This is best accomplishe d by identifying which of the hypoglycemic processes is involved, as t reatments differ. Some patients present with hypoglycemia and liver me tastases; among them, only a few develop hypoglycemia as a result of a failure of hepatic glucose production. Most develop hypoglycemia as a result of an insulin-mediated process-either the secretion of insulin by an islet-cell tumor or the secretion of insulin-like growth factor -II by an extrapancreatic tumor. Administration of glucagon can rapidl y make the two groups distinguishable, thus allowing institution of th erapy and prompt symptomatic control of hypoglycemia. METHODS. The cha rts of seven patients with tumor hypoglycemia and liver metastases who had a glucagon stimulation test (serial glucose measurements after a 1 mg infusion of glucagon) as part of the workup for hypoglycemia were retrospectively reviewed. Those patients whose test revealed a rise i n serum glucose of >30 mg/dL were subsequently treated as outpatients, with a continuous glucagon infusion delivered by a portable pump. RES ULTS. Three patients had an insulinoma and four had non-islet cell tum or hypoglycemia (NICTH) due to hepatocellular carcinoma, colon carcino ma, meningeal sarcoma, and hemangiopericytoma, respectively. All of th e patients had liver metastateses. Evaluation of these patients includ ed a glucagon stimulation test (1 mg intravenous push), which quickly provided information about the mechanism of tumor hypoglycemia and the direction towards therapy. All patients with insulinoma responded to glucagon with a rise in blood serum glucose levels, indicating adequat e glycogen stores. The four patients with NICTH had mixed responses: i n two patients, the response suggested that hypoglycemia was due to an insulin-like tumor product; glucose levels did not rise in the other two cases, indicating that hypoglycemia was due to poor hepatic glycog en reserve/liver failure. In all cases, a glycemic response to glucago n predicted good response to long term treatment with glucagon (0.06-0 .3 mg/hour, via intravenous infusion pump). CONCLUSIONS. The glucagon stimulation test is a simple and fast approach that serves to clarify the etiology of hypoglycemia (diagnostic use) and guide effective long term strategies for its control (therapeutic use) in patients with ne oplastic diseases and liver metastases. (C) 1998 American Cancer Socie ty.